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High-intensity interval training improves cardiac function by miR-206 dependent HSP60 induction in diabetic rats

  • ObjectiveA role for microRNAs is implicated in several biological and pathological processes. We investigated the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on molecular markers of diabetic cardiomyopathy in rats. MethodsEighteen male Wistar rats (260 +/- 10 g; aged 8 weeks) with streptozotocin (STZ)-induced type 1 diabetes mellitus (55 mg/kg, IP) were randomly allocated to three groups: control, MICT, and HIIT. The two different training protocols were performed 5 days each week for 5 weeks. Cardiac performance (end-systolic and end-diastolic dimensions, ejection fraction), the expression of miR-206, HSP60, and markers of apoptosis (cleaved PARP and cytochrome C) were determined at the end of the exercise interventions. ResultsBoth exercise interventions (HIIT and MICT) decreased blood glucose levels and improved cardiac performance, with greater changes in the HIIT group (p < 0.001, eta(2): 0.909). While the expressions of miR-206 and apoptotic markers decreased in bothObjectiveA role for microRNAs is implicated in several biological and pathological processes. We investigated the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on molecular markers of diabetic cardiomyopathy in rats. MethodsEighteen male Wistar rats (260 +/- 10 g; aged 8 weeks) with streptozotocin (STZ)-induced type 1 diabetes mellitus (55 mg/kg, IP) were randomly allocated to three groups: control, MICT, and HIIT. The two different training protocols were performed 5 days each week for 5 weeks. Cardiac performance (end-systolic and end-diastolic dimensions, ejection fraction), the expression of miR-206, HSP60, and markers of apoptosis (cleaved PARP and cytochrome C) were determined at the end of the exercise interventions. ResultsBoth exercise interventions (HIIT and MICT) decreased blood glucose levels and improved cardiac performance, with greater changes in the HIIT group (p < 0.001, eta(2): 0.909). While the expressions of miR-206 and apoptotic markers decreased in both training protocols (p < 0.001, eta(2): 0.967), HIIT caused greater reductions in apoptotic markers and produced a 20% greater reduction in miR-206 compared with the MICT protocol (p < 0.001). Furthermore, both training protocols enhanced the expression of HSP60 (p < 0.001, eta(2): 0.976), with a nearly 50% greater increase in the HIIT group compared with MICT. ConclusionsOur results indicate that both exercise protocols, HIIT and MICT, have the potential to reduce diabetic cardiomyopathy by modifying the expression of miR-206 and its downstream targets of apoptosis. It seems however that HIIT is even more effective than MICT to modulate these molecular markers.zeige mehrzeige weniger

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Metadaten
Verfasserangaben:Maryam Delfan, Raheleh Amadeh Juybari, Sattar Gorgani-Firuzjaee, Jens Høiriis Nielsen, Neda Delfan, Ismail Laher, Ayoub Saeidi, Urs GranacherORCiDGND, Hassane Zouhal
DOI:https://doi.org/10.3389/fcvm.2022.927956
ISSN:2297-055X
Pubmed ID:https://pubmed.ncbi.nlm.nih.gov/35845054
Titel des übergeordneten Werks (Englisch):Frontiers in cardiovascular medicine
Verlag:Frontiers Media
Verlagsort:Lausanne
Publikationstyp:Wissenschaftlicher Artikel
Sprache:Englisch
Datum der Erstveröffentlichung:29.06.2022
Erscheinungsjahr:2022
Datum der Freischaltung:18.06.2024
Freies Schlagwort / Tag:apoptosis; cardiomyopathy; diabetes; exercise; miRNAs
Band:9
Aufsatznummer:927956
Seitenanzahl:11
Fördernde Institution:Deutsche Forschungsgemeinschaft (DFG, German Research Foundation); [491466077]; Open Access Publishing Fund of the University of Potsdam,; Germany; Alzahra University
Organisationseinheiten:Humanwissenschaftliche Fakultät / Strukturbereich Kognitionswissenschaften / Department Sport- und Gesundheitswissenschaften
DDC-Klassifikation:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit
Peer Review:Referiert
Publikationsweg:Open Access / Gold Open-Access
DOAJ gelistet
Lizenz (Deutsch):License LogoCC-BY - Namensnennung 4.0 International
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